ECSS Paris 2023: CP-PN05
INTRODUCTION: Skeletal muscle is a plastic tissue that regenerates ad integrum after injury thanks to the key role of muscle stem cells (MuSCs) and their dynamic interactions with their niche (e.g., macrophages and fibro-adipogenic progenitors (FAP)). Skeletal muscle regeneration is improved in females as compared with males and is impaired in the absence of estrogens (1). One cause of sexual dimorphism in skeletal muscle regeneration may be therefore the natural fluctuations of estrogens during the ovarian cycle. So far, animal studies have used supraphysiological and constant estrogen doses in ovarian-hormone depleted females, thereby limiting our understanding on how the natural fluctuations of estrogens affect muscle regeneration. Here, we assessed the impact of ovarian cycle on skeletal muscle regeneration in adult male and female C57Bl6/J mice using a standardized model of muscle injury (2). METHODS: The ovarian cycle was controlled by smear analysis. Female mouse muscles were injured either in proestrus or estrus so that muscle regeneration takes place during the decrease or increase of circulating estrogen concentration, respectively. Muscle injury was also induced in males. Several days following the injury, maximal force production was evaluated to assess functional recovery, and histological analyses were performed to examine associated cellular changes. Additionally, loss-of-function experiments were conducted using a specific estrogen inhibitor. RESULTS: We showed a faster recovery of force production, considered as the best indirect marker of regeneration (3), for estrus females as compared with proestrus females and males. We also found a higher number of proliferating MuSCs in injured estrus females as compared with both injured males and proestrus females. In addition, the number of macrophages was lower and the number of FAPs was higher in injured females than in injured males, independently of the ovarian cycle. Interestingly, both skeletal force recovery and MuSC regulation were impaired in mice treated with a specific estrogen inhibitor. CONCLUSION: Overall, we concluded that cyclic variations of estrogens play a key role in skeletal muscle regeneration. Further studies are warranted to decipher the underlying cellular and molecular mechanisms. References (1) Jomard et al., Physiol Rep. 2023 Oct;11(19):e15798 (2) Bernard et al., FASEB J. 2023 Sep;37(9):e23107. (3) Paulsen et al., Exerc Immunol Rev. 2012;18:42-97.
Read CV JULIEN GONDINECSS Paris 2023: CP-PN05
INTRODUCTION: The heritability of strength- and power-based phenotypes has been investigated extensively, particularly in team sport athletes. However, few attempts have been made to investigate how these traits influence in-game performance, especially in rugby union (RU). RU is an intermittent, contact-intensive sport, made up of distinct playing positions, each with a diverse set of physiological demands. Adenosine monophosphate (AMP) deaminase is a key regulator of skeletal muscle energy metabolism. The C34T (rs17602729) polymorphism brings about a reduction in AMP deaminase activity in skeletal muscle via a C-to-T transition in the AMPD1 gene, converting a glutamine codon into a premature stop codon. It is plausible that reduced AMP deaminase activity would be inhibitory to elite RU performance via premature fatigue. As such, we aimed to identify whether AMPD1 C34T (rs17602729) genotype was associated with elite RU athlete status, playing position, and in-game performance. METHODS: The study included 621 male RU athletes and 1029 male and female non-athletes, all European ancestry. Athletes were organised into groups (forwards and backs) and subgroups relating to playing position. All athletes had competed in ≥5 matches in the highest league in a major rugby-playing nation and were thus classified as elite. Real-time PCR using TaqMan reagents determined genotype. Performance data for 347 athletes were obtained via Stats Perform OPTA (2012/13 to 2019/20 seasons), with metrics relating to both attack and defence. Due to low N of TT genotypes, CT and TT genotypes were grouped in some analyses. P values for multiple comparisons were subject to Benjamini-Hochberg correction to control for false discovery rate (5%). RESULTS: No differences in genotype or allele frequencies between athletes and non-athletes were observed. RU athletes of CC genotype played 13% longer per game than CT genotypes, and CC forwards played 13% longer per game than T allele carriers. In front 5 forwards, CC genotypes played 26% longer per game than T allele carriers. CC centres played 12% longer per game than T allele carriers. Interestingly, front 5 T allele carriers made 75% more clean breaks than CC genotypes. CONCLUSION: More minutes per appearance observed in CC genotypes suggests impaired fatigue resistance in T allele carriers. The improved performance of T allele carriers in front 5 forwards is surprising, suggesting a compensatory mechanism that allows those athletes to perform despite AMP deaminase deficiency. In conclusion, ascension to the elite level of RU is possible regardless of AMPD1 C34T polymorphism and performance is mostly unaffected, but RU players of CC genotype play more minutes per game.
Read CV Daniel MartinECSS Paris 2023: CP-PN05
INTRODUCTION: Tactical athletes require multi-domain fitness for selection and operational readiness, combining strength, power, aerobic capacity, severe-intensity tolerance, and cognitive-motor functioning. Within Special Operations Forces (SOF), individuals must meet minimal competence across all domains but typically display distinct performance strengths. Fitness in the sense of being fit for SOF tasks may therefore be described by emergent performance phenotypes. Alpha-actinin 3 (ACTN3) R577X is a well-established genetic marker linked to fast-twitch muscle structure and power-oriented performance in sport populations. However, it remains unclear whether ACTN3 variation is reflected in power-dominant phenotype profiles within elite tactical cohorts. METHODS: Baseline performance data from 236 SOF candidates and operators across 10 police and military units were aggregated into five standardized domains: strength, power, severe-intensity tolerance, aerobic endurance, and reaction time. Principal component analysis was used to derive a reduced multidimensional phenotype space, followed by k-means clustering (k=3) on principal components (PC) 1–3 scores to identify performance archetypes. Bayes factors quantified whether ACTN3 genotype frequencies differed across clusters. Cluster-specific genotype proportions and uncertainty intervals were summarized using Dirichlet-multinomial posterior estimates. RESULTS: PC1–PC3 explained 75.4% of the variation across the five fitness domains (PC1: 31.3%, PC2: 24.5%, PC3: 19.5%). PC1 reflected a neuromuscular capacity axis dominated by strength, severe-intensity tolerance, and power, PC2 primarily captured reaction time with a secondary aerobic endurance component, and PC3 reflected aerobic endurance specialization relative to power. ACTN3 genotype frequencies differed decisively across phenotype clusters (BF10 = 505). In the power-strength cluster (C3), 78.3% of individuals carried the ACTN3 CC (sometimes called ACTN3 RR) genotype (95% credible interval 68.9–86.4%), indicating a markedly higher CC frequency than in the other clusters, whereas the endurance-oriented cluster (C1) showed a higher relative frequency of the ACTN3 TT (or XX) genotype. Pairwise contrasts confirmed maximal separation between C1 and C3 (BF10 = 3.79). CONCLUSION: ACTN3 CC genotype is enriched in power-dominant performance phenotypes in elite tactical athletes. This provides first evidence that ACTN3 aligns with multidomain readiness phenotypes in a mixed-demand population, without deterministic interpretation, and with relevance for elite sport contexts requiring concurrent strength, power, endurance, and rapid decision-making.
Read CV Alain DösseggerECSS Paris 2023: CP-PN05